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Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.

ABSTRACT: Left stellate ganglion (LSG) hyperactivity promotes ischemia induced ventricular arrhythmia (VA). Blocking the Nav1.8 channel decreases neuron activity. Therefore, the present study aimed to investigate whether blocking the Nav1.8 channel with its specific blocker A-803467 in the LSG reduces sympathetic activity and exerts anti-arrhythmic effects. Forty canines were divided into dimethylsulfoxide (DMSO) group and 10?mM, 15?mM, and 20 mM A-803467 groups. A volume of 0.1?ml of A-803467 or DMSO was injected into the LSG. The ventricular electrophysiological parameters, LSG function were measured before and 30?min after the injection. VA was assessed for 60?min after ischemia and then LSG tissues were collected for molecular biological experiments. Compared with DMSO, concentration-dependent prolonged action potential duration and effective refractory period, decreased LSG function were identified after A-803467 treatment. Moreover, the severity of ischemia induced VA was decreased in A-803467 groups. Furthermore, decreased nerve growth factor, decreased c-fos and increased sympathetic neuron apoptosis were found in the LSG after A-803467 injection. In conclusion, blocking the Nav1.8 channel could significantly attenuate ischemia-induced VA, primarily by suppressing LSG activity.

SUBMITTER: Yu L

PROVIDER: S-EPMC5428783 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.

Yu Lilei L Wang Menglong M Hu Dan D Huang Bing B Zhou Liping L Zhou Xiaoya X Wang Zhuo Z Wang Songyun S Jiang Hong H

Scientific reports 20170403 1

Left stellate ganglion (LSG) hyperactivity promotes ischemia induced ventricular arrhythmia (VA). Blocking the Nav1.8 channel decreases neuron activity. Therefore, the present study aimed to investigate whether blocking the Nav1.8 channel with its specific blocker A-803467 in the LSG reduces sympathetic activity and exerts anti-arrhythmic effects. Forty canines were divided into dimethylsulfoxide (DMSO) group and 10 mM, 15 mM, and 20 mM A-803467 groups. A volume of 0.1 ml of A-803467 or DMSO was ...[more]

PMID: 28373696

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Project description:BackgroundAnti-mitochondrial antibody (AMA)-positive myositis is an atypical inflammatory myopathy characterized by chronic progression of muscle atrophy and cardiac involvement. Few detailed reports have shown the clinical course of the cardiac complications of AMA-positive myositis.Case summaryA 47-year-old man presented with shortness of breath on exertion. Cardiac dilatation was visible on chest X-ray, and echocardiography demonstrated diffuse hypokinesis with a reduced left ventricular (LV) ejection fraction of 30%. He had mild muscle weakness in the bilateral iliopsoas muscles, and his creatine kinase (CK) and anti-mitochondrial M2 antibody levels were elevated. A liver biopsy showed no findings of primary biliary cholangitis. Coronary angiography revealed normal coronary arteries. An endomyocardial biopsy showed interstitial fibrosis and marked degeneration of the mitochondria. Fluorodeoxyglucose (FDG)-positron emission tomography/computed tomography showed circumferential abnormal accumulation in the LV myocardium, and he was diagnosed with cardiomyopathy associated with AMA-positive myositis. Optimal drug therapy for heart failure was started, and a cardiac resynchronization therapy-defibrillator was implanted. However, his cardiac function did not improve, and he was hospitalized due to ventricular tachycardia storm 5 years after the diagnosis. Ventricular tachycardia was terminated by radiofrequency catheter ablation on the LV-anterior papillary muscle. Steroid therapy was initiated and resulted in a decreased uptake of FDG and a normalized CK level at 3 months after his second discharge; however, LV systolic dysfunction remained 1 year later.DiscussionAnti-mitochondrial antibody-positive myositis can affect the myocardium and cause severe LV dysfunction and life-threatening ventricular arrhythmia over time.KeywordsAnti-mitochondrial antibody-positive myositis • Endomyocardial biopsy • Ventricular tachycardia • Left ventricular dysfunction • Case report • Magnetic resonance imaging • Near-infrared spectroscopy-intravascular ultrasound.

Dataset Information

Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.

Publications

Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.

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